Evidence map›Paper›PMID 27230536›Full record

ArticleScientific reports2016

Innate immune responses in human hepatocyte-derived cell lines alter genotype 1 hepatitis E virus replication efficiencies.

Pradip B Devhare, Swapnil Desai, Kavita S Lole

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

26 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. A novelJHEP reports : innovation in hepatology · 2025
    Article
  4. Liver diseases: epidemiology, causes, trends and predictions.Signal transduction and targeted therapy · 2025
    Review
  5. Article
  6. Hepatitis E virus: from innate sensing to adaptive immune responses.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  7. Article
  8. Article
  9. Immunobiology and Host Response to HEV.Advances in experimental medicine and biology · 2023
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Pradip B DevhareHepatitis Division, National Institute of Virology, Microbial Containment Complex, Pashan, Pune, India.
Swapnil DesaiHepatitis Division, National Institute of Virology, Microbial Containment Complex, Pashan, Pune, India.
Kavita S LoleHepatitis Division, National Institute of Virology, Microbial Containment Complex, Pashan, Pune, India.
ICMR-National Institute of Virology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatitis E virus (HEV) is a significant health problem in developing countries causing sporadic and epidemic forms of acute viral hepatitis. Hepatitis E is a self-limiting disease; however, chronic HEV infections are being reported in immunocompromised individuals. The disease severity is more during pregnancy with high mortality (20-25%), especially in third trimester. Early cellular responses after HEV infection are not completely understood. We analyzed innate immune responses associated with genotype-I HEV replication in human hepatoma cell lines (Huh7, Huh7.5 and HepG2/C3A) using HEV replicon system. These cells supported HEV replication with different efficiencies due to the cell type specific innate immune responses. HepG2/C3A cells were less supportive to HEV replication as compared to Huh7.5 and S10-3 cells. Reconstitution of the defective RIG-I and TLR3 signaling in Huh7.5 cells enabled them to induce higher level antiviral responses and restrict HEV replication, suggesting the involvement of both RIG-I and TLR3 in sensing HEV RNA and downstream activation of interferon regulatory factor 3 (IRF3) to generate antiviral responses. Inhibition of IRF3 mediated downstream responses in HepG2/C3A cells by pharmacological inhibitor BX795 significantly improved HEV replication efficiency implying the importance of this study in establishing a better cell culture system for future HEV studies.

Indexed as

Immunity, InnateVirus ReplicationCarcinoma, HepatocellularCell Line, TumorDEAD Box Protein 58Gene ExpressionHepatitis E virusHepatocytesHumansInterferon Regulatory FactorsLiver NeoplasmsReceptors, ImmunologicReceptors, Pattern RecognitionSignal TransductionToll-Like Receptor 3TranscriptomeDEAD Box Protein 58Interferon Regulatory FactorsReceptors, ImmunologicReceptors, Pattern RecognitionRIGI protein, humanTLR3 protein, humanToll-Like Receptor 3

Identifiers

PMID27230536
PMCPMC4882509
OpenAlexW2399759182

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.